DETECTION OF ZONAL RENAL ISCHEMIA WITH CONTRAST-ENHANCED MR IMAGING WITH A MACROMOLECULAR BLOOD POOL CONTRAST AGENT

被引：21

作者：

VEXLER, VS ^{[1
]}

BERTHEZENE, Y ^{[1
]}

CLEMENT, O ^{[1
]}

MUHLER, A ^{[1
]}

ROSENAU, W ^{[1
]}

MOSELEY, ME ^{[1
]}

BRASCH, RC ^{[1
]}

机构：

[1] UNIV CALIF SAN FRANCISCO,DEPT RADIOL,513 PARNASSUS AVE,SAN FRANCISCO,CA 94143

来源：

JMRI-JOURNAL OF MAGNETIC RESONANCE IMAGING | 1992年 / 2卷 / 03期

关键词：

CONTRAST ENHANCEMENT; CONTRAST MEDIA; EXPERIMENTAL STUDIES; GADOLINIUM; KIDNEY; FAILURE; MR; MICROCIRCULATION IMAGING;

D O I：

10.1002/jmri.1880020311

中图分类号：

R8 [特种医学]; R445 [影像诊断学];

学科分类号：

1002 ; 100207 ; 1009 ;

摘要：

The potential of magnetic resonance (MR) imaging enhanced with albumin-(gadolinium diethylenetriaminepentaacetic acid [DTPA])35, a macromolecular blood pool marker, for detection of focal changes in renal perfusion was studied in a myoglobinuric acute renal failure (ARF) model in the rat. T1-weighted spin-echo postcontrast images of injured kidneys at 3 hours after glycerol injection showed three distinct zones: a strongly enhanced outer cortex, a low-intensity inner cortex, and a strongly enhanced medulla. The distinct band of low intensity in the inner cortex indicated zonal decreased blood volume, corresponding to published microsphere data showing zonal low perfusion in the inner cortex. Contrast differences between parenchymal zones were significant for at least 30 minutes. No focal ischemic changes could be delineated on nonenhanced images. Enhanced and nonenhanced images of injured kidneys obtained at 24 hours after glycerol injection revealed no zonal differentiation. Contrast-enhanced MR imaging data in this ARF model correlated well with pathologic data and microsphere perfusion results. Contrast-enhanced characterization of the ischemic phase of renal injury with MR imaging may improve specificity for the diagnosis of ARF and may serve as a marker for therapeutic intervention.

引用

页码：311 / 319

页数：9

共 29 条

[1]

Lordon RE, Burton JR, Post‐traumatic renal failure in military personnel in S.E. Asia, Am J Med, 53, pp. 73-86, (1972)

[2]

Hostetter TH, Brenner BM, Renal circulation and nephron function in experimental acute renal failure, Acute renal failure, pp. 67-89, (1988)

[3]

Kurtz TM, Maletz RM, Hsu C-H, Renal cortical blood flow in glycerol‐induced acute renal failure in the rat, Circ Res, 38, pp. 30-35, (1976)

[4]

Hsu C-H, Kurtz TW, Waldinger TP, Cardiac output and renal blood flow in glycerol‐induced acute renal failure in the rat, Circ Res, 40, pp. 178-182, (1977)

[5]

Reineck HJ, O'Connor GJ, Lifschitz MD, Stein JH, Sequential studies on the pathophysiology of glycerol‐induced acute renal failure, J Lab Clin Med, 96, pp. 357-362, (1980)

[6]

Hsu C-H, Kurtz TW, Sands CE, Intrarenal vascular resistance in glycerol‐induced acute renal failure in the rat, Circ Res, 45, pp. 583-587, (1979)

[7]

Thiel G, Wilson DR, Arce ML, Oken DE, Glycerol induced hemoglobinuric acute renal failure in the rat. II. The experimental model, predisposing factors, and pathophysiologic features, Nephron, 4, pp. 276-297, (1967)

[8]

Hsu C-H, Kurtz TW, Renal hemodynamics in experimental acute renal failure, Nephron, 27, pp. 204-208, (1981)

[9]

Mason J, The pathophysiology of ischaemic acute renal failure: a new hypothesis about the initial phase, Renal Physiol, 9, pp. 129-147, (1986)

[10]

Mason J, Welsch J, Takabatake T, Disparity between surface and deep nephron function early after renal ischemia, Kidney Int, 24, pp. 27-36, (1983)

← 1 2 3 →